Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.22.32 (bromelain)
1,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spleen and peritoneal cells from unimmunized BALB/c mice were cultured in the presence of LPS for 24 hr and fused to produce hybridomas secreting antibodies against bromelain-treated mouse erythrocytes (BrMRBC). Three clones from spleen cells and eight clones from peritoneal cells were isolated and characterized further. All the monoclonal antibodies had IgMK isotype. Their reactivities against untreated and bromelain-treated erythrocytes from various species were assessed by hemolysis and indirect radioimmunoassay; all the clones had similar antigen specificities. On the isoelectric focussing patterns of light chains, they were separated into two groups, two and nine clones, and all the light chains in each group showed identical patterns. The two groups shared no common idiotope detectable by anti-idiotype antibodies prepared by immunization of rabbits with the monoclonal antibodies, but all the antibodies in each group shared common idiotopes. In each group, one antibody had a unique idiotope different from any other antibody, but eight antibodies in a group shared another identical idiotope. These findings suggest the restricted heterogeneity of anti-BrMRBC antibodies in the mouse.
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PMID:Mouse monoclonal antibodies against bromelain-treated mouse erythrocytes: reactivity with erythrocytes of various species of animals and idiotypes. 310 56

Spleen cells from normal, nonautoimmune mice (C3H/HeN) spontaneously produce hemolytic plaques against autologous bromelain-treated red blood cells (BrMRBC). The number of anti-BrMRBC plaques detectable can be increased by including either a 3 M KCl extracted antigen from BrMRBCs or the hapten phosphorylcholine chloride (PC) as an antigenic analog in the plaque assay. Optimal PC concentration for augmenting the number of plaque forming cells (PFCs) was between 10(-7) and 10(-8) M. Incubation of spleen cells with an equal volume of 10(-7) M PC one, two, or three times resulted in the preparation of populations of cells which yielded increased numbers of PFCs. In addition, the number of anti-BrMRBC plaques of cells incubated three times could not be further increased by adding PC to the plaquing mixture. The eluate produced by the initial incubation of spleen cells with 10(-7) M PC specifically suppressed the anti-BrMRBC PFC response of these nonhapten augmentable cell populations (3 X eluted). These studies indicate that a naturally occurring autoantibody response is normally regulated by the presence of a molecule bound to the cell surface of autoantibody forming cells.
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PMID:Demonstration of hapten augmentable plaques in the bromelain treated anti-mouse red blood cell system: putative evidence for anti-idiotypic regulation of autoantibody secretion. 352 50

Mice injected with rat red blood cells (RBC), or rat bromelain-treated (brom) RBC, produce RBC autoantibodies and suppressor cells that specifically inhibit the autoimmune response without inhibiting the net production of antibodies against rat RBC. It has been investigated whether suppressor cells induced by injections of rat RBC are effective in preventing autoantibody production induced by rat brom RBC and vice versa. Autoantibodies were induced in C3H mice by weekly ip injections, each 0.2 ml, of a 6% suspension of rat RBC or rat brom RBC. Autoantibody production was assayed using Coombs' test. Suppressor cells were present in the spleens of mice positive in Coombs' tests and were shown by intravenous injections of 40 X 10(6) viable cells per mouse into untreated syngeneic mice 18 hr before the first injection of rat RBC or rat brom RBC. Autoantibodies eluted from mice positive in Coombs' tests after injections of rat RBC or brom RBC were absorbed by either type of rat RBC but not by RBC from sheep. This suggests that rat RBC and rat brom RBC display antigens that are similar, if not identical, to autoantigens on the mouse RBC. Spleen cells from mice injected with rat RBC suppressed autoantibodies induced by both rat RBC and rat brom RBC. In contrast, spleen cells from mice injected with rat brom RBC suppressed autoantibodies induced by rat brom RBC but not those induced by unmodified rat RBC. This differential suppression may be due to the removal from rat RBC, by bromelain, of a suppressor site and/or autoantigens of some specificities. Thus rat brom RBC may not induce the total range of specificities of autoantibodies, and of suppressor cells, induced by rat RBC.
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PMID:Experimental erythrocyte autoantibodies. V. Induction and suppression of red blood cell autoantibodies in mice injected with rat bromelain-treated red blood cells. 622 25

Spleen, lymph node, and peripheral blood lymphocytes from healthy guinea pigs (gp) were examined for their ability to produce polyreactive autoantibodies to a battery of self-antigens and to cryptic determinants (phosphatidylcholine) on bromelain-treated mouse red blood cells (Br-MRBC). The mouse monoclonal antibody (Mab) 8BE6 anti-gp pan-T (CD5) marker was used for identification of CD5+ B1 cells by the plaque-forming assay (PFC), immunofluorescence, complement-mediated cytotoxicity, and immunocytochemistry. The detection of CD5+ cells by the 8BE6 Mab depended on the method used. They were better demonstrated by cytolysis and immunocytochemistry than by FACS analysis. By the latter method, the level of the CD5+ B cell subpopulation was associated neither with the age of the gp nor with the organ examined. Similarly wide ranges of PFC were detected in untreated or LPS-treated animals regardless of age and organ. The vast majority of the LPS-stimulated IgM antibody-secreting B lymphocytes reacting with the Br-MRBC, and those producing natural autoantibodies, did not bind the 8BE6 Mab.
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PMID:CD5+ and CD5- B1-like lymphocytes in healthy guinea pig. 934 96